Evidence map›Paper›PMID 41032750›Full record

ArticleBlood2026

Mucosal calprotectin is associated with severity of aGI-GVHD and poor outcomes after allogeneic stem cell transplantation.

Ekin Ece Gurer Kluge, Elisabeth Meedt, Julia Feicht, Kedi Cao, Andreas Hiergeist, Andreas Mamilos, Daniela Hirsch, Matthias Hoepting, Anna-Sophia Kattner, Carina Matos and 16 more

Abstract read
In one paragraph

Article in Blood, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Article
  2. Observational
  3. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

26 authors.

Ekin Ece Gurer KlugeClinic and Polyclinic for Internal Medicine III, University Hospital Regensburg, Regensburg, Germany.ORCID 0000-0002-1758-9814
Elisabeth MeedtClinic and Polyclinic for Internal Medicine III, University Hospital Regensburg, Regensburg, Germany.
Julia FeichtClinic and Polyclinic for Internal Medicine III, University Hospital Regensburg, Regensburg, Germany.
Kedi CaoClinic and Polyclinic for Internal Medicine III, University Hospital Regensburg, Regensburg, Germany.ORCID 0000-0002-1018-9463
Andreas HiergeistInstitute of Clinical Microbiology and Hygiene, University Hospital Regensburg, Regensburg, Germany.ORCID 0000-0002-3154-0638
Andreas MamilosDepartment of Pathology, University of Regensburg, Regensburg, Germany.
Daniela HirschDepartment of Pathology, University of Regensburg, Regensburg, Germany.
Matthias HoeptingClinic and Polyclinic for Internal Medicine III, University Hospital Regensburg, Regensburg, Germany.
Anna-Sophia KattnerClinic and Polyclinic for Internal Medicine III, University Hospital Regensburg, Regensburg, Germany.ORCID 0000-0002-5438-6995
Carina MatosClinic and Polyclinic for Internal Medicine III, University Hospital Regensburg, Regensburg, Germany.
Sigrid BülowInstitute of Clinical Microbiology and Hygiene, University Hospital Regensburg, Regensburg, Germany.ORCID 0000-0002-8952-290X
Erik Thiele OrbergClinic and Polyclinic for Internal Medicine III, University Hospital Regensburg, Regensburg, Germany.ORCID 0000-0003-1969-8261
Philipp BeckhoveLeibniz Institute for Immunotherapy, Regensburg, Germany.ORCID 0000-0002-0099-5576
Arne KandulskiDepartment of Internal Medicine I, Gastroenterology, Hepatology, Endocrinology, Rheumatology, and Infectious Disease, University Hospital Regensburg, Regensburg, Germany.ORCID 0009-0005-9065-8395
Matthias EvertDepartment of Pathology, University of Regensburg, Regensburg, Germany.
Kai HildnerDepartment of Medicine 1, University Hospital Erlangen, University of Erlangen-Nuremberg, Kussmaul Campus for Medical Research, Erlangen, Germany.ORCID 0000-0001-5007-4874
Marina KreutzClinic and Polyclinic for Internal Medicine III, University Hospital Regensburg, Regensburg, Germany.
Matthias EdingerClinic and Polyclinic for Internal Medicine III, University Hospital Regensburg, Regensburg, Germany.
Daniel WolffClinic and Polyclinic for Internal Medicine III, University Hospital Regensburg, Regensburg, Germany.ORCID 0000-0001-7015-3190
Wolfgang HerrClinic and Polyclinic for Internal Medicine III, University Hospital Regensburg, Regensburg, Germany.
Hendrik PoeckClinic and Polyclinic for Internal Medicine III, University Hospital Regensburg, Regensburg, Germany.
André GessnerInstitute of Clinical Microbiology and Hygiene, University Hospital Regensburg, Regensburg, Germany.
Daniela WeberClinic and Polyclinic for Internal Medicine III, University Hospital Regensburg, Regensburg, Germany.
Birte KehrLeibniz Institute for Immunotherapy, Regensburg, Germany.ORCID 0000-0002-3417-7504
Ernst HollerClinic and Polyclinic for Internal Medicine III, University Hospital Regensburg, Regensburg, Germany.
Sakhila GhimireClinic and Polyclinic for Internal Medicine III, University Hospital Regensburg, Regensburg, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

abstractCalprotectin, a calcium- and zinc-binding protein that comprises the subunits S100A8 and S100A9, has been extensively studied as a biomarker of gastrointestinal (GI) inflammation through fecal and serum analyses. However, its role in intestinal tissue remains poorly understood because of the limited availability of biopsy specimens. In this study, we analyzed S100A8 and S100A9 messenger RNA (mRNA) expression in 579 intestinal biopsy specimens from allogeneic stem cell transplantation recipients and observed a strong association with acute GI graft-versus-host disease (aGI-GVHD; P< .001). Neutrophil infiltration correlated with the severity of aGI-GVHD (P< .001), and calprotectin expression was strongly linked to Toll-like receptor 4 (TLR4; P< .001) and TLR2 (P< .001) expression. Both TLR4 and aGI-GVHD were associated with elevated calprotectin mRNA levels (P< .001). When patients received broad-spectrum antibiotics at disease onset, calprotectin expression was suppressed (S100A8, P = .001; S100A9, P = .01). GI site-specific differences in calprotectin expression were identified: during severe aGI-GVHD, levels increased up to 30-fold in the small intestine and up to fivefold in the large intestine with respect to mild or no aGI-GVHD, whereas under homeostasis, the large intestine exhibited higher baseline calprotectin (P = .001). The high clinical relevance of this finding is evident from the observation that calprotectin expression was prognostic for transplant-related mortality. Our study suggests that (1) calprotectin is a potential biopsy biomarker in aGI-GvHD and (2) calprotectin expression and neutrophil infiltration possibly indicate translocation of microbiota, which (3) may be modulated by antibiotics.

Indexed as

Graft vs Host DiseaseHematopoietic Stem Cell TransplantationIntestinal MucosaLeukocyte L1 Antigen ComplexAdolescentAdultAgedBiomarkersCalgranulin ACalgranulin BFemaleHumansMaleMiddle AgedRNA, MessengerSeverity of Illness IndexBiomarkersCalgranulin ACalgranulin BLeukocyte L1 Antigen ComplexRNA, MessengerS100A8 protein, humanS100A9 protein, humanTLR2 protein, humanTLR4 protein, humanToll-Like Receptor 2Toll-Like Receptor 4

Identifiers

PMID41032750
PMCPMC12917305

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.